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Ca 2+ store‐dependent potentiation of Ca 2+ ‐activated non‐selective cation channels in rat hippocampal neurones in vitro
Author(s) -
Partridge L. Donald,
Valenzuela C. Fernando
Publication year - 1999
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1999.00617.x
Subject(s) - long term potentiation , chemistry , biophysics , metabotropic glutamate receptor , ampa receptor , metabotropic receptor , glutamate receptor , hippocampal formation , ryanodine receptor , schaffer collateral , excitatory postsynaptic potential , acpd , neuroscience , biology , biochemistry , intracellular , receptor
1 Potentiation of calcium‐activated non‐selective cation (CAN) channels was studied in rat hippocampal neurones. CAN channels were activated by IP 3 ‐dependent Ca 2+ release following metabotropic glutamate receptor (mGluR) stimulation either by Schaffer collateral input to CA1 neurones in brain slices in which ionotropic glutamate and GABA A receptors, K + channels, and the Na + ‐Ca 2+ exchanger were blocked or by application of the mGluR antagonist ACPD in cultured hippocampal neurones. 2 The CAN channel‐dependent depolarization (Δ V CAN ) was potentiated when [Ca 2+ ] i was increased in neurones impaled with Ca 2+ ‐containing microelectrodes. 3 Fura‐2 measurements revealed a biphasic increase in [Ca 2+ ] i when 200 μ m ACPD was bath applied to cultured hippocampal neurones. This increase was greatly attenuated in the presence of Cd 2+ . 4 Thapsigargin (1 μ m ) caused marked potentiation of Δ V CAN in CA1 neurones in the slices and of the CAN current ( I CAN ) measured in whole cell‐clamped cultured hippocampal neurones. 5 Ryanodine (20 μ m ) also led to a potentiation of Δ V CAN while neurones pretreated with 100 μ m dantrolene failed to show potentiation of Δ V CAN when impaled with Ca 2+ ‐containing microelectrodes. 6 The mitochondrial oxidative phosphorylation uncoupler carbonyl cyanide m ‐chlorophenyl hydrazone (2 μ m ) also caused a potentiation of Δ V CAN . 7 CAN channels are subject to considerable potentiation following an increase in [Ca 2+ ] i due to Ca 2+ release from IP 3 ‐sensitive, Ca 2+ ‐sensitive, or mitochondrial Ca 2+ stores. This I CAN potentiation may play a crucial role in the ‘amplification’ phase of excitotoxicity.